Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1003265 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25565900_1.fastq.gz | Fastqsanger.gz | |||
| SRR25565900_2.fastq.gz | Fastqsanger.gz | |||
| SRR25565873_1.fastq.gz | Fastqsanger.gz | |||
| SRR25565873_2.fastq.gz | Fastqsanger.gz | |||
| SRR25565874_1.fastq.gz | Fastqsanger.gz |
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Project description:Interventions: case series:None
Primary outcome(s): postoperative cognitive dysfunction;IL-6;IL-1;Gut flora
Study Design: Cohort study
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Project description:Cognitive impairment (CI) is a prevalent neurological condition characterized deficient attention, causal reasoning, learning and/or memory. Many genetic and environmental factors increase risk for CI, and the gut microbiome is increasingly implicated. However, the identity of gut microbes associated with CI risk, their effects on CI, and their mechanisms of action remain unclear. Here we examine the gut microbiome in response to restricted diet and intermittent hypoxia, known environmental risk factors for CI. Modeling the environmental factors together in mice potentiates CI and alters the gut microbiota. Depleting the microbiome by antibiotic treatment or germ-free rearing prevents the adverse effects of environmental risk on CI, whereas transplantation of the risk-associated microbiome into naïve mice confers CI. Parallel sequencing and gnotobiotic approaches identify the pathobiont Bilophila wadsworthia as enriched by the environmental risk factors for CI and as sufficient to induce CI. Consistent with CI-related behavioral abnormalities, B. wadsworthia and the risk-associated microbiome disrupt hippocampal activity, neurogenesis and gene expression. The CI induced by B. wadsworthia and by environmental risk factors is associated with microbiome-dependent increases in intestinal IFNy-producing Th1 cells. Inhibiting Th1 cells abrogates the adverse effects of both B. wadsworthia and environmental risk factors on CI. Together, these findings identify select gut bacteria that contribute to environmental risk for CI in mice by promoting inflammation and hippocampal dysfunction.
2021-04-01 | GSE163099 | GEO
Project description:Alzheimers disease and epilepsy are reciprocally related. Among sporadic AD patients, seizures occur in 10-22 percent, and subclinical epileptiform abnormalities occur in 22-5 percent. Cognitive deficits, with prominent short-term memory impairments, occur in most epilepsy patients. Common neurophysiological and molecular mechanisms occur in AD and epilepsy. Emerging evidence identifies choroid plexus pathological changes in aging, AD, and epilepsy. These include decreased CSF turnover, A-beta and tau accumulation with impaired clearance, and disrupted CSF amino acid homeostasis; this pathology may contribute to synaptic dysfunction in AD and epilepsy.
We found altered signaling pathways in the choroid plexus of severe AD cases and many correlated changes in protein expression of cell metabolism pathways in AD and epilepsy cases. Shared molecular mechanisms should be investigated further to distinguish pathogenic from secondary changes. This could inform novel therapeutic strategies to prevent disease progression or restore normal function. Focusing on dual-diagnosed AD/epilepsy cases, specific epilepsy syndromes like temporal lobe epilepsy, and changes across different severity levels in AD and epilepsy would significantly add to our understanding.
2023-02-27 | MSV000091370 | MassIVE
Project description:Changes in gut microbiota have been implicated in patients' pathophysiology and cognitive capabilities suffering from autism spectrum disorder. Yet, factors that mediate this interaction remain not fully understood. In this study, we analyzed stool samples from autistic pediatric patients and healthy individuals. Using multi-omics platforms, we characterized microbiota diversities, proteins, and possible altered metabolic pathways.
2021-07-14 | MSV000087817 | MassIVE
Project description:This descriptive, cross-sectional study will evaulate and fully characterize factors associated with cognitive dysfunction in Breast Cancer (BCS) and Colorectal Cancer (CRC) survivors that have cognitive concerns, and factors associated with psychoneurological symptom cluster in BCS and CRC survivors.
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Project description:Pancreatic cancer is the 3rd most prevalent cause of cancer related deaths in United states alone, with over 55000 patients being diagnosed in 2019 alone and nearly as many succumbing to it. Late detection, lack of effective therapy and poor understanding of pancreatic cancer systemically contributes to its poor survival statistics. Obesity and high caloric intake linked co-morbidities like type 2 diabetes (T2D) have been attributed as being risk factors for a number of cancers including pancreatic cancer. Studies on gut microbiome has shown that lifestyle factors as well as diet has a huge effect on the microbial flora of the gut. Further, modulation of gut microbiome has been seen to contribute to effects of intensive insulin therapy in mice on high fat diet. In another study, abnormal gut microbiota was reported to contribute to development of diabetes in Db/Db mice. Recent studies indicate that microbiome and microbial dysbiosis plays a role in not only the onset of disease but also in its outcome. In colorectal cancer, Fusobacterium has been reported to promote therapy resistance. Certain intra-tumoral bacteria have also been shown to elicit chemo-resistance by metabolizing anti-cancerous agents. In pancreatic cancer, studies on altered gut microbiome have been relatively recent. Microbial dysbiosis has been observed to be associated with pancreatic tumor progression. Modulation of microbiome has been shown to affect response to anti-PD1 therapy in this disease as well. However, most of the studies in pancreatic cancer and microbiome have remained focused om immune modulation. In the current study, we observed that in a T2D mouse model, the microbiome changed significantly as the hyperglycemia developed in these animals. Our results further showed that, tumors implanted in the T2D mice responded poorly to Gemcitabine/Paclitaxel (Gem/Pac) standard of care compared to those in the control group. A metabolomic reconstruction of the WGS of the gut microbiota further revealed that an enrichment of bacterial population involved in drug metabolism in the T2D group.
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Project description:Changes in gut microbiota have been implicated in patients' pathophysiology and cognitive capabilities suffering from autism spectrum disorder. Yet, factors that mediate this interaction remain not fully understood. In this study, we analyzed stool samples from autistic pediatric patients and healthy individuals. Using multi-omics platforms, we characterized microbiota diversities, proteins, and possible altered metabolic pathways.
2021-07-14 | MSV000087817 | GNPS
Project description:Changes in gut microbiota have been implicated in pathophysiology and cognitive capabilities of patients suffering from autism spectrum disorder. Yet, factors that mediate this interaction remain not fully understood. In this study, we analyzed stool samples from sever autistic pediatric patients and healthy individuals. Using multi omics platforms, we characterized microbiota diversities, proteins, and possible altered metabolic pathways.
2025-01-29 | PXD026274 | Pride
Project description:Background: The long-term high-fat, high-sugar diet exacerbates type 2 diabetes mellitus (T2DM)-related cognitive impairments. The negative impact of poor dietary patterns on brain development and neurological function may be related to gut microbiota disturbance. The role of phlorizin in mitigating glucose and lipid metabolism disorders is well documented. However, the protective effect of phlorizin on diabetes-related cognitive dysfunction is unclear. Therefore, the present study aimed to investigate the effect of dietary supplementation of phlorizin on high-fat and high-fructose diet (HFFD)-induced cognitive dysfunction and evaluate the crucial role of the microbiota-gut-brain axis. Results: Dietary supplementation of phlorizin for 14 weeks effectively prevented glucolipid metabolism disorder, spatial learning impairment, and memory impairment in HFFD mice. In addition, phlorizin improved the HFFD-induced decrease in synaptic plasticity, neuroinflammation, and excessive activation of microglia in the hippocampus. Transcriptomics analysis shows that the protective effect of phlorizin on cognitive impairment was associated with increased expression of neurotransmitters and synapse-related genes in the hippocampus. Phlorizin treatment alleviated colon microbiota disturbance, mainly manifested by an increase in gut microbiota diversity and the abundance of short-chain fatty acid (SCFA)-producing bacteria. The level of microbial metabolites, including SCFA, inosine 5'-monophosphate (IMP), and D (-)-beta-hydroxybutyric acid (BHB) were also significantly increased after phlorizin treatment. Moreover, integrating multiomics analysis observed tight connections between phlorizin-regulated genes, microbiota, and metabolites. Furthermore, removal of the gut microbiota via antibiotics treatment diminished the protective effect of phlorizin against HFFD-induced cognitive impairment, underscoring the critical role of the gut microbiota in mediating cognitive behavior. Importantly, supplementation with SCFA and BHB alone mimicked the regulatory effects of phlorizin on cognitive function. Conclusions: These results indicate that gut microbiota and their metabolites mediate the ameliorative effect of phlorizin on HFFD-induced cognitive impairment. Therefore, phlorizin can be used as an easy-to-implement nutritional therapy to prevent and alleviate metabolism-related neurodegenerative diseases by targeting the regulation of the microbiome-gut-brain axis.
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